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Proliferating Resident Microglia after Focal Cerebral Ischaemia in Mice
Abstract
Cerebral ischaemia usually results in the rapid death of neurons within the immediate territory of the affected artery. Neuronal loss is accompanied by a sequence of events, including brain oedema, blood-brain barrier (BBB) breakdown, and neuroinflammation, all of which contribute to further neuronal death. Although the role of macrophages and mononuclear phagocytes in the expansion of ischaemic injury has been widely studied, the relative contribution of these cells, either of exogenous or intrinsic central nervous system (CNS) origin is still not entirely clear. The purpose of this study, therefore, was to use different durations of transient middle cerebral artery occlusion (tMCAo) in the mouse to investigate fully post-occlusion BBB permeability and cellular changes in the brain during the 72 h post-MCAo period. This was achieved using in vivo magnetic resonance imaging (MRI) and cell labelling techniques. Our results show that BBB breakdown and formation of the primary ischaemic damage after tMCAo is not associated with significant infiltration of neutrophils, although more are observed with longer periods of MCAo. In addition, we observe very few infiltrating exogenous macrophages over a 72 h period after 30 or 60 mins of occlusion, instead a profound increase in proliferating resident microglia cells was observed. Interestingly, the more severe injury associated with 60 mins of MCAo leads to a markedly reduced proliferation of resident microglial cells, suggesting that these cells may play a protective function, possibly through phagocytosis of infiltrating neutrophils. These data further support possible beneficial actions of microglial cells in the injured brain.
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“Also, very few infiltrating exogenous macrophages were observed over the first 72 h period and, instead, a profound increase in proliferating resident microglia cells was observed (Denes et al., 2007).”
From The impact of microglial activation on blood-brain barrier in brain diseases (2014) · cites this paper as Denes et al., 2007
In the citing paper
“Denes and colleagues used cell tracking techniques and MRI imaging to describe that, despite of BBB breakdown caused by transient middle cerebral artery occlusion (tMCAo), the infiltration of neutrophils was more prominent only in longer periods of MCAo, with extensive BBB damage.”
From The impact of microglial activation on blood-brain barrier in brain diseases (2014) · cites this paper as Denes et al., 2007
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Metadata
- Authors
- Denes, A., Vidyasagar, R., Feng, J., Narvainen, J., McColl, B. W., Kauppinen, R. A., & Allan, S. M.
- Affiliations
- Laboratory of Molecular Neuroendocrinology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary
- University of Birmingham (GB)
- Chinese Academy of Sciences (CN)
- Faculty of Life Sciences, Michael Smith Building, University of Manchester, Manchester, UK
- University of Manchester (GB)
- Venue
- Journal of Cerebral Blood Flow & Metabolism
- Publisher
- SAGE Publications
- Published
- 2007-12
- Volume
- 27
- Issue
- 12
- Pages
- 1941-1953
- ISSN
- 0271-678X (ISSN-L)
- 1559-7016
- OpenAlex
- W2001952628
- Cited by
- 342
- References
- 40
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 9 · 2023: 17 · 2022: 17 · 2021: 36 · 2020: 14 · 2019: 22 · 2018: 27 · 2017: 17 · 2016: 33 · 2015: 23 · 2014: 18 · 2013: 28 · 2012: 19
- FWCI
- 8.26
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Cerebral Blood Flow & Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Research Explorer (The University of Manchester) (publishedVersion)
- University of Birmingham Research Portal (University of Birmingham) (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Health Sciences › Medicine › Clinical Neurology › Acute Ischemic Stroke Management
- Keywords
- microglial proliferation, focal cerebral ischemia, transient middle cerebral artery occlusion, blood-brain barrier disruption, neutrophil infiltration, macrophage infiltration, neuroinflammation, phagocytosis, neuroprotection, ischemic injury
- MeSH terms
- Animals, Antimetabolites, Bromodeoxyuridine, Ischemic Attack, Transient, Data Interpretation, Statistical, Dextrans, Fluorescent Antibody Technique, Iron, Macrophages, Magnetic Resonance Imaging, Male, Mice, Inbred C57BL, Monocytes, Oxides, Phagocytes, Microglia, Infarction, Middle Cerebral Artery, Neutrophil Infiltration, Cell Proliferation, Mice, Ferrosoferric Oxide, Magnetite Nanoparticles
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